Glaucoma is usually associated with an elevation of the pressure within the eye (or intraocular pressure), which usually results from an abnormality in outflow channel, (i.e., an increased resistance in the trabecular meshwork). It is generally accepted that the extracellular compartment of the trabecular meshwork (TM) plays an important role in the outflow pathway of the eye. For this reason, searching for the cause of the outflow reduction in this extracellular environment has been the major interest in many glaucoma research labs nationwide. Our lab has taken a combined approach including cellular, molecular biology and biochemical techniques to identify and isolate specific and major extracellular changes in human TM cells. Our lab has identified a candidate gene which codes for an extracellular molecule synthesized by trabecular meshwork cells. The substantial induction of this molecule is caused by steroid treatment of the HTM cells and the pattern of the induction matches the intraocular pressure progressive induction experienced by patients after 10 to 15 days of steroid therapy. By a cloning approach, we have isolated the gene and expressed the protein in a baculovirus system. To further explore the possible relationship of this protein with steroid glaucoma, we need characterize the molecule and investigate its interactions with other extracellular components and enzymes. The computer graphics equipment and programming facilities available in the UCSF Computer Graphics Laboratory are powerful tools that will aid us in studying the structure, functions and interactions of the protein with other molecules.